In the last year we have completed two functional neuroimaging studies examining the central control of vocalization during the perception and production of speech and non-speech sounds. A great deal of controversy in the field has developed around the possibility that the neural control for human speech involves specialized brain mechanisms that have emerged separate from animal vocalizations. In mammalian communication stereotyped cries are used to warn of danger, isolation cries of infants, and to express pain and pleasure. This system is also present in humans as well as speech for communication. In this study, event related functional MRI with sparse sampling measured blood oxygenation dependent levels in the emotional vocalization systems and the cortical speech system during perception, planning and production of two sets of behaviors, speech and non-speech. For speech we used nonsense syllables /bem/-/dauk/, /hik/-/ld /, /saip/-/kuf/, /lok/-/chim/, and /raig/-/sot/, devoid of lexicality and following the rules of English phonology. For non-speech we used familiar sounds such cough-sigh, sing (/a/ on a tone)-raspberry, kiss-snort, laugh-tongue click, and whistle-cry. Results showed substantial activation overlap between speech and non-speech brain activation in regions supporting auditory-motor integration in the left hemisphere. Both the speech and non-speech tasks produced the same pattern of brain activation primarily in the left hemisphere involving the frontal operculum and the temporoparietal structures previously reported to support speech production. Although non-speech showed greater extent and amplitude of activation in the regions examined, both speech and non-speech showed comparable left laterality in activation for perception and production. These findings posit a more general role of the auditory dorsal stream in the left hemisphere in supporting vocal tract gestures with auditory targets that are not limited to speech processing. [unreadable] [unreadable] The Section has focused for many years on two idiopathic speech disorders that are thought to be neurological based; developmental stuttering and spasmodic dysphonia. Both are task specific disorders only affecting speech in that emotional vocalization such as cry, laughter and shout are not affected and symptoms are apparent only during speech for communication. In stuttering, speech is dysfluent for communication purposes while singing and other vocalizations are not affected. We hypothesized that the pattern of brain activation would be altered from normal in adults who stutter during the perception, planning and production of speech but not during asymptomatic perception, planning and production of non-speech vocalizations. During both speech and non-speech perception and planning, stuttering speakers had less activation relative to controls in the frontal and temporoparietal regions. During speech and non-speech production, the stuttering speakers had less activation in the left STG, and the left pre-motor areas (BA 6), but had greater activation relative to controls in the right STG, bilateral HG, insula, putamen, and precentral motor regions (BA 4). The results demonstrated decreased sensorimotor activation during the perception and planning of both speech and non-speech targets in stuttering speakers. During speech and non-speech production, the stuttering speakers had increased activation in primary and secondary auditory areas particularly on the right but less activation in the sensory and motor regions in the left hemisphere. These results were similar for both speech and nonspeech, demonstrating that neural activation differences in stuttering speakers are not speech-specific. [unreadable] [unreadable] Several voice disorders may develop secondary to dopamine depletion. Hypophonia is a common early symptom in Parkinson disease (PD) and spasmodic dysphonia (SD) is a voice disorder with laryngeal hypertonicity. Some patients first develop SD with PD emerging several years later suggesting that SD may be an early manifestation of partial dopamine depletion. Our aim is to determine the effects of dopamine neurotransmission blockade on the laryngeal physiology induced by selective dopamine receptor antagonists; SCH 23390 a specific D1 receptor antagonist, eticlopride a specific D2 receptor antagonist and when combined (SCH23390 + eticlopride) in the rat. Under alpha-chloralose anesthesia, the laryngeal thyroarytenoid (TA) muscles and the gastrocnemius (GN) muscles were recorded while stimulating either side of the internal branch of superior laryngeal nerve containing afferents for the laryngeal adductor response to elicit the laryngeal adductor response (LAR) in 5 conditions: pre-saline (1), post-saline (2), pre-drug (3, either SCH23390, eticlopride or SCH23390+eticlopride), 5min post-drug (4) and 1hr post-drug (5). Our results showed resting activity of the TA muscles increased significantly in the SCH23390 group but not in other two groups and no changes in GN muscle tone were found. LAR latency decreased (P < 0.01) and magnitude increased (P<0.01) in both SCH23390 and SCH23390+eticlopride groups, but no changes occurred in the eticlopride group. This study demonstrated that D1 receptor neurotransmission, but not D2, serves to suppress laryngeal muscle activity, reduce the amplitude and delay muscle responses to afferent input making the system less responsive to sensory triggers in the upper airway. In addition, effects of D1 receptors on laryngeal motor neurons differed from limb muscles. The results suggest that consideration should be given to selective modulation of D1 receptors for the treatment of laryngeal disorders in parkinsonism, and might improve hypophonia in these patients.